Mechanisms of AD neurodegeneration may be independent of Aβ and its derivatives.
about
Transthyretin and the brain re-visited: is neuronal synthesis of transthyretin protective in Alzheimer's disease?Presenilin-1 regulates the expression of p62 to govern p62-dependent tau degradationAmyloid beta precursor protein and prion protein have a conserved interaction affecting cell adhesion and CNS developmentAcetyl-CoA the key factor for survival or death of cholinergic neurons in course of neurodegenerative diseasesMild cognitive impairment: pathology and mechanisms.Cellular mechanisms of γ-secretase substrate selection, processing and toxicityInconsistencies and controversies surrounding the amyloid hypothesis of Alzheimer's diseaseIntracellular amyloid and the neuronal origin of Alzheimer neuritic plaquesEvidence of a novel mechanism for partial γ-secretase inhibition induced paradoxical increase in secreted amyloid β proteinSystematic review of the relationship between amyloid-β levels and measures of transgenic mouse cognitive deficit in Alzheimer's disease.Brain metabolic dysfunction at the core of Alzheimer's disease.Coexistence of phases in a protein heterodimerSystematic analysis of time-dependent neural effects of soluble amyloid β oligomers in culture and in vivo: Prevention by scyllo-inositol.Cell signaling abnormalities may drive neurodegeneration in familial Alzheimer diseaseAβ mediates Sigma receptor degradation via CaN/NFAT pathwayPresenilin-1/γ-secretase controls glutamate release, tyrosine phosphorylation, and surface expression of N-methyl-D-aspartate receptor (NMDAR) subunit GluN2B.Amyloid-independent mechanisms in Alzheimer's disease pathogenesisPharmacologists and Alzheimer disease therapy: to boldly go where no scientist has gone before.The paradox of syndromic diversity in Alzheimer disease.Fe65 matters: new light on an old molecule.Allelic interference: a mechanism for trans-dominant transmission of loss of function in the neurodegeneration of familial Alzheimer's disease.Dissecting Complex and Multifactorial Nature of Alzheimer's Disease Pathogenesis: a Clinical, Genomic, and Systems Biology Perspective.Conformational landscape of an amyloid intra-cellular domain and Landau-Ginzburg-Wilson paradigm in protein dynamics.Twenty Years of Presenilins--Important Proteins in Health and Disease.Defective Transcytosis of APP and Lipoproteins in Human iPSC-Derived Neurons with Familial Alzheimer's Disease Mutations.Amyloid beta: structure, biology and structure-based therapeutic development.Presenilin 1 promotes trypsin-induced neuroprotection via the PAR2/ERK signaling pathway. Effects of presenilin 1 FAD mutations.Presenilin mediates neuroprotective functions of ephrinB and brain-derived neurotrophic factor and regulates ligand-induced internalization and metabolism of EphB2 and TrkB receptors.Mechanisms linking brain insulin resistance to Alzheimer's disease.Interplay Between the Autophagy-Lysosomal Pathway and the Ubiquitin-Proteasome System: A Target for Therapeutic Development in Alzheimer's Disease.
P2860
Q21202832-ECF1D853-58F9-42C4-9702-9A21844CE1C0Q24296704-1E31E0B9-5E0E-493C-8E5B-44FF8D684D7DQ24305972-2D1D06FE-BE69-4D6C-A7A7-A5A8F19BD9E2Q24608842-2A0DDF9A-1911-4318-A4DE-52C5B896B010Q24631255-3A33AECF-C6D7-49CE-8ED8-CE17A3D903A7Q26859108-48776CF7-B9EE-4096-91CE-32EF3695653CQ27003841-BDC4D57F-51A4-463B-B8CF-F5A665DF469AQ34266573-1979F5A3-8156-4DDB-9693-1F0DCD02920BQ35128180-AA7CB121-F202-41A9-94CC-21E9444EA775Q35137134-3932300F-789B-44F6-8458-434A7D99F711Q35997881-5B39729E-308E-4FE3-8D56-7F1DBEEDA5F8Q36139267-A73C1042-3D7A-41A8-8664-563F58278CDEQ36269014-5065CB39-0CA4-4115-9325-E7963491F769Q37033913-99F55AE6-80E0-41B7-81E7-1C4EE038960FQ37227991-F36877E6-2532-4184-A612-EE19C44F2C96Q37234077-F8EB907B-951C-439B-86A8-C37D71E1BDACQ37808579-E836E46D-2DFB-459A-92CD-CA7D61743AFEQ37910243-63551A54-B252-42D1-8BD6-DEBD5BF32DCFQ38026786-7EFAA7A7-E606-43E6-AFF4-034BC6B3939AQ38057997-76DDBCE1-C086-495D-87A6-C5B71D5D5D5FQ38147958-FF3F4FF8-74B6-4F05-B124-1193D5F11E6FQ38583222-B1781835-40EB-462D-806F-26EB86B20D5BQ38836106-10A2F504-02B2-4DCB-9437-50410A90E1E3Q38938820-396F453C-E0B8-4E09-B258-306DD6B1DBF9Q39298977-8289349D-7845-4A34-923B-3C469B49AB82Q39437881-76AD273E-6A2D-4517-8972-5163DC3E2927Q39796754-554D9C8E-7A81-454D-A494-0A2F9429F30EQ42022663-5DE4ED03-28F9-4795-9CFE-4FEF7EDB35F8Q47113718-D1D9D6B6-A3C1-464F-B199-52A7EB15D76AQ55231947-67D4367C-2AF5-4A65-91EA-278B26D35528
P2860
Mechanisms of AD neurodegeneration may be independent of Aβ and its derivatives.
description
2010 nî lūn-bûn
@nan
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
2010年论文
@zh
2010年论文
@zh-cn
name
Mechanisms of AD neurodegeneration may be independent of Aβ and its derivatives.
@ast
Mechanisms of AD neurodegeneration may be independent of Aβ and its derivatives.
@en
type
label
Mechanisms of AD neurodegeneration may be independent of Aβ and its derivatives.
@ast
Mechanisms of AD neurodegeneration may be independent of Aβ and its derivatives.
@en
prefLabel
Mechanisms of AD neurodegeneration may be independent of Aβ and its derivatives.
@ast
Mechanisms of AD neurodegeneration may be independent of Aβ and its derivatives.
@en
P2860
P1476
Mechanisms of AD neurodegeneration may be independent of Aβ and its derivatives.
@en
P2093
Nikolaos K Robakis
P2860
P304
P356
10.1016/J.NEUROBIOLAGING.2010.05.022
P577
2010-07-01T00:00:00Z